ABSTRACT
Objective To investigate the effects of dexmedetomidine (DEX) on the mRNA expression of triggering receptor expressed on myeloid cells 1 (TREM-1) in peripheral blood mononuclear cells of rats with acute obstructive suppurative cholangitis (AOSC).Methods Sixty healthy male Wistar rat models of AOSC induced by complete common bile duct ligation and injection of E.coli into the bile duct through an intubation tube were replicated successfully.After modeling,the peripheral blood was collected and mononuclear cells were isolated and cultured.According to random number table method,the mononeuclear cells were divided into model group (no drug added in culture of mononuclear cells) and low,medium and high dose DEX groups (final concentrations 0.4,0.8,1.2 μg/L DEX were in low,medium and high DEX mononuclear cell cultures,respectively).After the mononuclear cells were cultured for 24 hours,the levels of tumor necrosis factor-α (TNF-α),interleukins (IL-1 and IL-6) in the supernatant of the cultured mononuclear cells were detected by enzyme linked immunosorbent assay (ELISA).The level of C-reactive protein (CRP) was detected by immunity transmission turbidimetry.The expression of TREM-1 mRNA in the mononuclear cells was detected by reverse trantscription-polymerase chain reaction (RT-PCR).Results Compared with the model group,the levels of TNF-α,IL-1,IL-6,CRP were decreased,the TREM-1 mRNA expressions were down-regulated in the different DEX dose groups,and the degrees of descent in medium and high dose groups were more significant than those in low dose group [TNF-oα (ng/L):95.5±8.6,88.9±5.3 vs.131.1 ± 14.2;IL-1 (ng/L):53.5±8.3,48.3 ± 6.7 vs.73.7 ± 12.8;IL-6 (ng/L):266.9±26.2,252.1 ± 17.7 vs.349.9±40.4;CRP (ng/L):4.3 ± 1.1,3.9 ±0.7 vs.5.6 ± 1.7;TREM-1 mRNA (A value):0.43 ± 0.18,0.39 ± 0.16 vs.0.65 ±0.25,all P ＜ 0.05].Conclusion DEX can down-regulate the expression of TREM-1 mRNA and inhibit the formation and secretion of inflammatory factors TNF-α,IL-1,IL-6 and CRP in peripheral blood mononuclear cells of rats with ASOC.